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Cited by 337Cellular Mechanics and InteractionsProtein Kinase Regulation and GTPase SignalingAxon Guidance and Neuronal Signaling

The Arp2/3 complex is required for lamellipodia extension and directional fibroblast cell migration

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Suraneni, Praveen, Rubinstein, Boris, Unruh, Jay R., Durnin, Michael, Hanein, Dorit, Li, Rong·2012·Journal of Cell Biology
DOI 10.1083/jcb.201112113PMC PMC3328382
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Abstract

The Arp2/3 complex nucleates the formation of the dendritic actin network at the leading edge of motile cells, but it is still unclear if the Arp2/3 complex plays a critical role in lamellipodia protrusion and cell motility. Here, we differentiated motile fibroblast cells from isogenic mouse embryonic stem cells with or without disruption of the ARPC3 gene, which encodes the p21 subunit of the Arp2/3 complex. ARPC3−/− fibroblasts were unable to extend lamellipodia but generated dynamic leading edges composed primarily of filopodia-like protrusions, with formin proteins (mDia1 and mDia2) concentrated near their tips. The speed of cell migration, as well as the rates of leading edge protrusion and retraction, were comparable between genotypes; however, ARPC3−/− cells exhibited a strong defect in persistent directional migration. This deficiency correlated with a lack of coordination of the protrusive activities at the leading edge of ARPC3−/− fibroblasts. These results provide insights into the Arp2/3 complex’s critical role in lamellipodia extension and directional fibroblast migration.

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  • ARP2/3-dependent lamellipodia formation promotes cell migration and invasion.

    “ARP2/3-dependent lamellipodia formation promotes cell migration and invasion (Molinie & Gautreau, 2018, Mondal et al., 2021, Suraneni, Rubinstein et al., 2012).”

    From SHARPIN S146 phosphorylation mediates ARP2/3 interaction, cancer cell invasion and metastasis (2022) · cites this paper as Suraneni, Rubinstein et al., 2012

    The Results and discussion section (page unavailable) shows that fibroblasts lacking ARPC3 fail to form lamellipodia and have impaired directional migration in wound-healing and EGF-gradient assays. The paper supports a role in directional fibroblast migration, but the cited claim also attributes promotion of invasion to it; our copy does not report an invasion finding. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Suraneni, P., Rubinstein, B., Unruh, J. R., Durnin, M., Hanein, D., & Li, R.
Affiliations
  • Stowers Institute for Medical Research (US)
  • Sanford Burnham Prebys Medical Discovery Institute (US)
Corresponding author
Li, Rong
ORCID
Venue
Journal of Cell Biology
Publisher
Rockefeller University Press
Published
2012-04-09
Volume
197
Issue
2
Pages
239-251
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
DOI
10.1083/jcb.201112113
PMC
PMC3328382
OpenAlex
W2058293976
Cited by
337
References
3
Citations by year
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FWCI
16.37
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Cell Biology (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
National Institute of General Medical Sciences (P01GM066311)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular Mechanics and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
Keywords
Arp2/3 complex, ARPC3, lamellipodia, fibroblast migration, directional cell migration, leading edge protrusion, formins, mDia1, mDia2, filopodia, cell motility, mouse embryonic stem cells
MeSH terms
Animals, Cell Differentiation, Cell Movement, Cells, Cultured, Female, Fibroblasts, Genotype, Male, Mice, Inbred C57BL, Pseudopodia, Wound Healing, Actin-Related Protein 2-3 Complex, Mice, Embryonic Stem Cells, Gene Knockout Techniques

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